• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

骨桥蛋白通过激活NF-κB信号通路促进根尖周炎中的骨破坏

Osteopontin Promotes Bone Destruction in Periapical Periodontitis by Activating the NF-κB Pathway.

作者信息

Dong Ming, Yu Xinxin, Chen Wanfang, Guo Zhenzhen, Sui Linlin, Xu Yuefei, Shang Yuhong, Niu Weidong, Kong Ying

机构信息

College of Basic Medical Sciences, Dalian Medical University, Dalian, China.

Department of Obstetrics and Gynecology of Renal Disease, the First Affiliated Hospital of Dalian Medical University, Dalian, China.

出版信息

Cell Physiol Biochem. 2018;49(3):884-898. doi: 10.1159/000493219. Epub 2018 Sep 5.

DOI:10.1159/000493219
PMID:30184545
Abstract

BACKGROUND/AIMS: Periapical periodontitis is caused by bacterial infection and results in both one destruction and tooth loss. Osteopontin (OPN) is a secreted phosphorylated glycoprotein that participates in bone metabolism.

METHODS

Thirty-three patients with chronic periapical periodontitis and 10 patients who had undergone the orthodontic removal of healthy tooth tissue (control) at the periodontal ligament were investigated, and an animal model of mouse periapical periodontitis was established for an in vivo analysis. The relationship between OPN and bone destruction during periapical periodontitis was analyzed. Osteoblasts and osteoclasts were cultured in vitro and treated with lipopolysaccharide. An inhibitor of NF-κB was used to pretreat the transfected cells.

RESULTS

OPN increased osteoclast proliferation and differentiation, but reduced osteoblasts proliferation and differentiation. OPN activated the NF-κB pathway during periapical periodontitis and accelerated the transfer and phosphorylation of P65 from the cytoplasm to the nucleus.

CONCLUSION

This study demonstrated that OPN played important roles in the progression of periapical periodontitis, and a dual role in bone metabolism during periapical periodontitis, linking osteoclasts and osteoblasts. The underlying mechanism may be related to the NF-κB pathway.

摘要

背景/目的:根尖周炎由细菌感染引起,会导致骨质破坏和牙齿脱落。骨桥蛋白(OPN)是一种分泌型磷酸化糖蛋白,参与骨代谢。

方法

对33例慢性根尖周炎患者和10例在牙周膜处正畸拔除健康牙齿组织的患者(对照组)进行研究,并建立小鼠根尖周炎动物模型用于体内分析。分析根尖周炎期间OPN与骨破坏之间的关系。体外培养成骨细胞和破骨细胞,并用脂多糖处理。使用NF-κB抑制剂对转染细胞进行预处理。

结果

OPN增加破骨细胞增殖和分化,但减少成骨细胞增殖和分化。OPN在根尖周炎期间激活NF-κB通路,并加速P65从细胞质向细胞核的转移和磷酸化。

结论

本研究表明,OPN在根尖周炎进展中起重要作用,在根尖周炎期间的骨代谢中起双重作用,连接破骨细胞和成骨细胞。其潜在机制可能与NF-κB通路有关。

相似文献

1
Osteopontin Promotes Bone Destruction in Periapical Periodontitis by Activating the NF-κB Pathway.骨桥蛋白通过激活NF-κB信号通路促进根尖周炎中的骨破坏
Cell Physiol Biochem. 2018;49(3):884-898. doi: 10.1159/000493219. Epub 2018 Sep 5.
2
OPN N-glycosylation promoted bone destruction.骨破坏中 OPN 的 N 糖基化作用。
Oral Dis. 2023 Jul;29(5):2154-2162. doi: 10.1111/odi.14218. Epub 2022 May 3.
3
Inhibition of RGS10 Aggravates Periapical Periodontitis via Upregulation of the NF-κB Pathway.RGS10 抑制通过上调 NF-κB 通路加重根尖周炎。
J Endod. 2022 Oct;48(10):1308-1318.e5. doi: 10.1016/j.joen.2022.07.009. Epub 2022 Aug 27.
4
Sesquiterpene lactone parthenolide blocks lipopolysaccharide-induced osteolysis through the suppression of NF-kappaB activity.倍半萜内酯小白菊内酯通过抑制核因子κB活性来阻断脂多糖诱导的骨溶解。
J Bone Miner Res. 2004 Nov;19(11):1905-16. doi: 10.1359/JBMR.040919. Epub 2004 Sep 27.
5
Nlrp3 inflammasome drives regulatory T cell depletion to accelerate periapical bone erosion.Nlrp3炎性小体促使调节性T细胞耗竭,从而加速根尖周骨侵蚀。
Int Endod J. 2024 Aug;57(8):1110-1123. doi: 10.1111/iej.14062. Epub 2024 Mar 5.
6
Involvement of interleukin‑23 induced by Porphyromonas endodontalis lipopolysaccharide in osteoclastogenesis.牙髓卟啉单胞菌脂多糖诱导的白细胞介素-23在破骨细胞生成中的作用
Mol Med Rep. 2017 Feb;15(2):559-566. doi: 10.3892/mmr.2016.6041. Epub 2016 Dec 14.
7
Interleukin-12-mediated expression of matrix metalloproteinases in human periodontal ligament fibroblasts involves in NF-κB activation.白细胞介素-12 介导的人牙周膜成纤维细胞基质金属蛋白酶的表达涉及 NF-κB 的激活。
Biosci Rep. 2017 Nov 21;37(6). doi: 10.1042/BSR20170973. Print 2017 Dec 22.
8
Role of the Btk-PLC2 Signaling Pathway in the Bone Destruction of Apical Periodontitis.BTK-PLC2 信号通路在根尖周炎骨破坏中的作用。
Mediators Inflamm. 2019 Jul 25;2019:8767529. doi: 10.1155/2019/8767529. eCollection 2019.
9
Monotropein attenuates ovariectomy and LPS-induced bone loss in mice and decreases inflammatory impairment on osteoblast through blocking activation of NF-κB pathway.芒柄花素通过抑制 NF-κB 通路的激活,减轻去卵巢和 LPS 诱导的小鼠骨丢失,并降低破骨细胞的炎症损伤。
Chem Biol Interact. 2018 Aug 1;291:128-136. doi: 10.1016/j.cbi.2018.06.015. Epub 2018 Jun 14.
10
Role of PI3K in the bone resorption of apical periodontitis.PI3K 在根尖周炎骨吸收中的作用。
BMC Oral Health. 2022 Aug 11;22(1):345. doi: 10.1186/s12903-022-02364-2.

引用本文的文献

1
Levels of matrix metalloproteinase-1 (MMP-1), MMP-2, MMP-3, osteopontin, pentraxin-3, and thymic stromal lymphopoietin in crevicular fluid samples from peri-implantitis, periodontitis, and healthy sites.种植体周围炎、牙周炎和健康部位龈沟液样本中基质金属蛋白酶-1(MMP-1)、MMP-2、MMP-3、骨桥蛋白、五聚素-3和胸腺基质淋巴细胞生成素的水平。
J Periodontal Res. 2025 May;60(5):473-483. doi: 10.1111/jre.13338. Epub 2024 Sep 26.
2
The role of NF-kappaB in the inflammatory processes related to dental caries, pulpitis, apical periodontitis, and periodontitis-a narrative review.NF-κB 在与龋齿、牙髓炎、根尖周炎和牙周炎相关的炎症过程中的作用——叙述性综述。
PeerJ. 2024 Aug 29;12:e17953. doi: 10.7717/peerj.17953. eCollection 2024.
3
Loricrin and Cytokeratin Disorganisation in Severe Forms of Periodontitis.
严重牙周炎中兜甲蛋白和细胞角蛋白的结构紊乱。
Int Dent J. 2023 Dec;73(6):862-872. doi: 10.1016/j.identj.2023.05.004. Epub 2023 Jun 12.
4
Screening of feature genes related to immune and inflammatory responses in periodontitis.筛选与牙周炎免疫和炎症反应相关的特征基因。
BMC Oral Health. 2023 Apr 21;23(1):234. doi: 10.1186/s12903-023-02925-z.
5
Expression of Toll-like receptor 2, Dectin-1, and Osteopontin in murine model of pulpitis.牙髓病小鼠模型中Toll样受体2、树突状细胞相关C型凝集素-1和骨桥蛋白的表达
Clin Oral Investig. 2023 Mar;27(3):1177-1192. doi: 10.1007/s00784-022-04732-2. Epub 2022 Oct 7.
6
Mechanisms of bone remodeling and therapeutic strategies in chronic apical periodontitis.慢性根尖周炎中骨改建的机制与治疗策略。
Front Cell Infect Microbiol. 2022 Jul 22;12:908859. doi: 10.3389/fcimb.2022.908859. eCollection 2022.
7
HMBOX1 attenuates LPS-induced periodontal ligament stem cell injury by inhibiting CXCL10 expression through the NF-κB signaling pathway.HMBOX1通过NF-κB信号通路抑制CXCL10表达,减轻脂多糖诱导的牙周膜干细胞损伤。
Exp Ther Med. 2022 Mar;23(3):224. doi: 10.3892/etm.2022.11148. Epub 2022 Jan 17.
8
The Crossroads of Periodontitis and Oral Squamous Cell Carcinoma: Immune Implications and Tumor Promoting Capacities.牙周炎与口腔鳞状细胞癌的交叉点:免疫影响与肿瘤促进能力
Front Oral Health. 2021 Jan 20;1:584705. doi: 10.3389/froh.2020.584705. eCollection 2020.
9
VISTA Blockade Aggravates Bone Loss in Experimental Murine Apical Periodontitis.VISTA 阻断加重实验性小鼠根尖周炎的骨丢失。
Front Immunol. 2021 Oct 7;12:738586. doi: 10.3389/fimmu.2021.738586. eCollection 2021.
10
Parathyroid hormone increases alveolar bone homoeostasis during orthodontic tooth movement in rats with periodontitis via crosstalk between STAT3 and β-catenin.甲状旁腺激素通过 STAT3 和 β-连环蛋白的串扰增加牙周炎大鼠正畸牙齿移动期间的肺泡骨稳态。
Int J Oral Sci. 2020 Dec 30;12(1):38. doi: 10.1038/s41368-020-00104-2.